7092

• UCREFRP Catalog Number: 7092
• Author: Eisler, R.
• Title: Arsenic Hazards to Fish, Wildlife, and Invertebrates
• USFW Year: 1988.
• USFW - Doc Type: A Synoptic Review.
• Copyright Material: NO

but may un?quple oxidative phosphorylation (Howard et al. 1984; EPA 1985).
Inorganic As interrupts oxidative metabolic pathways and sometimes causes
morphological changes in liver mitochondria. Arsenite in vitro reacts with
protein-SH groups to inactivate enzymes such as dihydrolipoyl dehydrogenase
and thiolase, producing inhibited oxidation of Ay ruvate and beta-oxidation of
fatty acids (Belton et al. 1985). Inorganic Asmay also exert toxic effects
by the reaction of arsenous acid (HAsO) with the sulfhydryl (SH) groups of
enzymes. In the first reaction, arsenous acid is reduced to arsonous acid
(AsOH ), which then condenses to either monothiols or dithiols to yield
dithigesters of arsonous acid. Arsonous acid may then condense with enzyme SH
groups to form a binary complex (Knowles and Benson 1984a,b).
Methylation to methylarsonic acid ((CH ) Aso H ) 'and dimethylarsinic acid
((CH ) Aso H) is usually the major deth?fic?t?on mechanism for inorganic
pent Mleni arsenates and trivalent arsenites in mammals. Methylated
arsenicals rapidly clear from all tissues except perhaps the thyroid
(Marafante et al. 1985; Vahter and Marafante 1985; Yamauchi et al. 1986).
Methylated arsenicals are probably common in nature. Methylation of arsenic
(unlike methylation of mercury) greatly reduces toxicity and is a true
detoxification process ?P olson 1975). ?Sfore methylation (which occurs
largely in the liver), As is reduced to As --the kidney being an important
site for this transformation (Belton et al. 1985). Arsenate reduction and
subsequent methylation is rapid: both arsenite and dimethylarsinate were
present in hgmster (Cricetus sp.) plasma only 12 minutes postinjection of
inorganic As (Hanlon and Ferm 1986c). Demethylation of methylated
arsenicals formed in vivo has not yet been reported (EPA 1980).
Toxic effects of organoarsenicals are exerted by initial metabolism to
the trivalent arsonoxide form, and then by reaction with sulfhydryl groups of
tissue proteins and enzymes to form an arylbis (organylthio) arsine (NAS
1977). This form, in turn, inhibits oxidative degradation of carbohydrates
and decreases cellular ATP, the energy storage molecule of the cell (NRCC
1978). Among the organoarsenicals, those physiologically most injurious are
methylarsonous acid (CH As(OH) ) and dimethylarsinous acid ((CH ) AsOH)
(Knowles and Benson 1984b). The 9nzyme inhibitory forms of organoarL Aicals
(arsonous acid) are formed from arsenous acid and the corresponding arsonic
acids by a wide variety of enzymes and subcellular particles (Knowles and
Benson 1984a). Organoarsenicals used as growth promoters and drugs are
converted to more easily excretable (and sometimes more toxic) substances,
although most organoarsenicals are eliminated without being converted to
inorganic arsenic or to demethylarsinic acids (Pershagen and Vahter 1979).
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